Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 41 patients with ischaemic heart disease and 30 normal donors were subjected to examinations of the biochemical indices of the blood coagulation system in its coagulation and anticoagulation links, as well as to tests reflecting the fibrinolytic and inhibitory activity of the urine. In the presence of thromboembolic complications in myocardial infarction patients a sharp elevation of "residual fibrinogen" and antiplasmins is noted along with a reduction of the urokinase activity of the urine.
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PMID:[Possibilities of early diagnosis of thromboembolic complications in myocardial infarct by means of biochemical methods]. 14 Feb 60

This study sought to determine whether clinical variables can be used to identify patients at high risk of recurrent spontaneous myocardial ischemia or hemodynamic compromise during the 1st 4 days after intravenous thrombolysis for acute myocardial infarction. Of 288 patients randomly assigned to a conservative postthrombolysis strategy, 54 (19%) required urgent cardiac catheterization within 24 h; 75 (26%) underwent urgent cardiac catheterization within 4 days of admission. Of the clinical variables examined by multiple logistic regression analysis, only patient age and anterior wall myocardial infarction correlated with the need for urgent cardiac catheterization (p = 0.0016 and p = 0.017, respectively). Compared with recombinant tissue-type plasminogen activator or urokinase monotherapy, combination therapy with these agents was associated with a lower need for acute intervention during the 1st 24 h after admission, but the difference did not reach statistical significance (14% for combination therapy vs. 21% for each agent alone, p = 0.30). Of the 75 patients undergoing urgent coronary angiography, only 39% had an occluded infarct-related artery. Emergency coronary angioplasty was performed in 49% of the patients and coronary artery bypass graft surgery was performed urgently in 3%. Despite these interventions, the need for urgent cardiac catheterization was associated with an in-hospital mortality rate of 7% (vs. 3% in the group not requiring urgent angiography, p = 0.36); mean left ventricular ejection fraction was 50.5 +/- 11% (vs. 54.3 +/- 10.8%, p = 0.12) and regional infarct zone wall motion was -2.68 +/- 1.07 SD/chord (vs. -2.46 +/- 1.19 SD/chord; p = 0.44).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Determinants of the need for early acute intervention in patients treated conservatively after thrombolytic therapy for acute myocardial infarction. TAMI-5 Study Group. 196 Mar 2

A 68-year-old man who presented with unstable angina had had cardiac bypass surgery 12 years earlier and successful angioplasty of a native circumflex lesion 18 months previously. Repeat catheterization showed a widely patent angioplasty site but interval closure of a saphenous vein graft to a large marginal branch that was totally occluded proximally. A stress test revealed significant myocardial ischemia. Severe peripheral peripheral vascular disease with known bilateral iliac artery occlusions mandated a brachial approach. Because of his high risk for repeat cardiac surgery, it was elected to attempt saphenous graft angioplasty following a prolonged urokinase infusion. After an infusion of urokinase for 36 hr, antegrade flow was restored and angioplasty was carried out successfully on a discrete mid-graft legion. Subsequent stress testing showed resolution of the ischemia. There were no vascular complications.
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PMID:Successful angioplasty of a chronically occluded saphenous vein graft using a prolonged urokinase infusion from the brachial route. 207 Mar 99

A 45-year-old man with unstable angina developed persistent ECG changes of myocardial ischemia during coronary angiography. Occlusion of the left anterior descending branch (LAD) was documented 20 minutes after these changes. Intracoronary nitrate, Ca antagonist, urokinase, removal by percutaneous transluminal coronary angioplasty (PTCA) of atherosclerotic obstructions, and emergency bypass surgery failed to restore myocardial perfusion. Only short periods of reflow were obtained by urokinase and PTCA. The repeated coronary injections demonstrated a progressive disappearance of the left anterior descending artery (LAD) starting from the distal portion and progressing retrogradely up to the origin of the vessel. The patient developed a transmural anterolateral myocardial infarction and 12 months later underwent cardiac transplantation for untractable failure. His heart was examined and the infarct confirmed. Analysis of this case suggests that coronary occlusion in acute myocardial infarction can be an event secondary to increased intramyocardial resistance rather than the cause of reduced coronary blood flow in subepicardial coronary arteries.
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PMID:Coronary occlusion: cause or consequence of acute myocardial infarction? 229 57

The current revolution in the treatment of acute myocardial infarction by means of thrombolytic therapy has as its underlying strategy three aims: early restoration of the blood flow in order to salvage jeopardized but still viable tissues; limitation of acute consequences of ischemic heart disease, such as infarct size, ventricular fibrillation, and pericardial effusion; and preservation, as far as possible, of ventricular function. It is also hoped that these three achievements will result in reduced short- as well as long-term mortality rates. The techniques employed in this overall strategy are still under investigation, and several leading pharmacological compounds vie for supremacy: streptokinase (SK) and its anisoylated form (APSAC), recombinant technique tissue type plasminogen activator (rt-PA), and urokinase (UK) with or without prourokinase (PUK). Other pharmacological agents, such as angiotensin converting enzyme (ACE) inhibitors, beta-blockers, Ca2+ antagonists, and O2 radical scavengers, might find here their "finest hour" yet. In addition, the underlying anatomy may require early or, where needed, delayed PTCA, backed up by coronary artery bypass grafting. Thus, the tactics of the intervention may vary from case to case and indeed from center to center depending on experience and facilities, but the strategic conclusion is clearly the same: early reperfusion is a must if one wishes to save ischemic but still viable tissue.
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PMID:Acute consequences of ischemic myocardial damage. 248 24

Early thrombolytic therapy has been shown to reduce hospital mortality after myocardial infarction by 20-50%. This is achieved through reperfusion of the ischemic myocardium, which leads to limitation of infarct size by 15-30% and preservation of regional and global left ventricular function. Thrombolysis and reperfusion can be achieved by intravenous administration of streptokinase, urokinase, APSAC, or rt-PA, or by intracoronary administration of streptokinase or urokinase. Thrombolytic therapy is most effective in patients with extensive myocardial ischemia (large infarction) treated early after the onset of symptoms, but also patients with smaller infarcts may benefit from the therapy. It is uncertain whether treatment later than six hours after the onset of symptoms is beneficial, and if so, in which patients. Thrombolytic therapy leads to bleeding complications in a minority of patients. The risk of intracranial bleeding is approximately 0.5%. However, in several large trials the rate of cerebrovascular accidents (bleeding plus embolism) was not higher after thrombolytic therapy with streptokinase or rt-PA than after placebo. In order to prevent rethrombosis, additional treatment with acetyl salicylic acid and heparin is recommended. Nitrates and antiarrhythmic drugs are not recommended as routine practice. Immediate PTCA does not improve patient outcome. At present angiography and subsequent angioplasty or bypass surgery is recommended in patients with recurrent ischemia (spontaneous or upon exercise) after the infarct.
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PMID:Thrombolytic therapy in acute myocardial infarction. 252 93

In open chest dogs myocardial ischemia was induced by formation of an occlusive thrombus in the left anterior circumflex artery (LCX). Reperfusion of the LCX was achieved by infusion of the fibrin specific recombinant single-chain urokinase-type plasminogen activator (r-scu-PA). The myocardial salvage by r-scu-PA alone and in combination with the epoprostenol (prostacyclin) analog taprostene (CG 4203) was compared. There were four experimental groups: group 1 (n = 4) did not receive any treatment after LCX thrombosis; in group 2 (n = 9) at 100 min after LCX thrombosis r-scu-PA (20 micrograms.kg-1.min-1 i.v. for 30 min) was infused; in groups 3 and 4 treatment with taprostene started concomitantly with r-scu-PA infusion. The taprostene infusions lasted for 120 min and the doses were 0.1 microgram.kg-1.min-1 in group 3 (n = 6) and 0.215 microgram.kg-1.min-1 in group 4 (n = 6). Time to r-scu-PA-induced recanalisation ranged from 18-22 min with no significant difference between groups 2-4. Percent of left ventricle at risk did not differ between the groups. Infarct size as percent of the risk zone was 48.3 +/- 7.7 in group 1, 25.3 +/- 3.7 in group 2, 21.3 +/- 6.5 in group 3 and 17.1 +/- 3.5 in group 4 (p less than 0.05 groups 2-4 vs group 1). Incidence of ectopic beats increased after r-scu-PA-induced reperfusion in groups 2-4, but was significantly reduced by taprostene.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Additional myocardial salvage by coadministration of the epoprostenol analog taprostene to recombinant single-chain urokinase-type plasminogen activator in a canine coronary thrombosis model. 266 59

In the past 20 years treatment appears to have had a major impact on all forms of cerebral vascular disease. Morbidity and mortality from strokes have declined nearly 50% in developed countries. Modern imaging techniques, methodology, and biostatistics have identified risk factors and refined clinical trials such that we question all previous studies of stroke management. Control of moderate and severe hypertension has significantly lowered stroke rates. In borderline and mild hypertension the decision to treat is influenced by other stroke risk factors including diabetes mellitus, cigarette smoking, ischaemic heart disease, plasma lipid levels, gout, haematocrit, and body weight. Current data indicate that anticoagulants are of no value, or hazardous, in atherothrombotic strokes; of unknown value in transient ischaemic attacks; of dubious value in evolving strokes; and beneficial in cardiac embolism. The cardiac causes, including mural thrombus, unstable arrhythmias, and mitral valve prolapse should be actively sought. Aspirin, as the prototype anti-platelet agent, holds promise in transient ischemic attacks and minor strokes at both small and moderate dosages. Ticlopine is now being critically evaluated in America. Use of cerebral vasodilators should be abandoned. Enthusiasm in the use of streptokinase and urokinase has been dampened by the conversion of ischemic infarcts into haemorrhagic infarcts. In subarachnoid haemorrhage epsilon-aminocaprioc acid is useful although hazardous, in preventing rebleeding. Certain calcium ion channel blockers are promising in the reduction of vasopasm. Since the November 1985 article in the new England Journal of Medicine on the failure of external-to-internal carotid arterial bypass to reduce the risk of ischemic stroke, the swing is back to conservative management.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Advances in the medical management of cerebral vascular disease. 331 47

Myocardial ischemia was induced by formation of an occlusive thrombus in the left anterior circumflex artery (LCX) in open chest dogs. The myocardial salvage by the fibrin specific recombinant single-chain urokinase-type plasminogen activator (r-scu-PA) alone and in combination with the oxygen radical scavenger human superoxide dismutase of recombinant origin (r-HSOD) was investigated. The three experimental groups were: group I (n = 4) did not receive any treatment after LCX thrombosis; in group II (n = 9) at 100 min after LCX thrombosis r-scu-PA (20 micrograms.kg1.min-1 i.v. for 30 min) was infused; dogs in group III (n = 8) received concomitant treatment with r-scu-PA and r-HSOD (10 mg.kg1 i.v. for 60 min). Percent of left ventricle at risk did not differ between the groups. Infarct size as percent of the risk zone was 45.3 +/- 8.0 in group I, 25.3 +/- 3.7 in group II (a less than or equal to 0.05 vs group I) and 14.9 +/- 3.2 in group III (a less than 0.05 vs group II). Incidence of reperfusion arrhythmias and increase in plasma creatine kinase were significantly diminished by r-HSOD when compared to dogs receiving r-scu-PA only. There were no significant differences in hemodynamic parameters between the groups. No changes in plasma fibrinogen were observed in r-scu-PA treated dogs. In conclusion, the combined treatment with r-scu-PA and r-HSOD yielded a significantly higher myocardial salvage versus thrombolytic treatment alone in a canine LCX thrombosis model.
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PMID:Enhanced myocardial salvage by combined treatment with recombinant single-chain urokinase-type plasminogen activator and recombinant human superoxide dismutase in a canine coronary thrombosis model. 336 72

Interventional angiographic techniques are of increasing importance in the management of arteriosclerosis and its complications. Two areas of particular interest are the treatment of focal arterial stenoses by percutaneous transluminal angioplasty and the treatment of arterial thromboemboli with selective infusion of thrombolytic agents. The administration of multiple drugs, in various combinations, is a critical factor in the success of these interventions. To effectively use this new pharmacoangiography, it is important to understand both the pathophysiology of the atherosclerotic or thrombotic process being treated and the actions of the drugs used. Preserving the effect of angioplasty relies on preventing thrombus formation and preventing recurrence of the atherosclerotic obstruction. Heparin during the procedure is clearly useful for the former, and aspirin in small doses and other antiplatelet medications are indicated for the latter. The precise utility of long-term anticoagulation, of low molecular weight dextran, and of various antiplatelet regimens remains to be proven. The theoretical importance of these medications in improving long-term patency rests on the effects they have on platelet and vessel wall prostaglandins, on intimal smooth muscle cell proliferation, and on the thrombogenicity of injured arterial intima. Fibrinolytic therapy, with streptokinase and urokinase, has been used for many years. Selective intraarterial use, however, is a new and promising application. Intracoronary streptokinase infusion during acute myocardial ischemia appears to prevent or limit infarction in certain patients. Peripheral use for acute arterial occlusion, either in native vessels or in grafts, is an area of great promise. Key considerations are thrombus age, size, and location, and the status of the arterial flow proximal and distal to the obstruction.
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PMID:Pharmacology of angioplasty and intravascular thrombolysis. 618 69


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